Discovering chemical modifiers of oncogene-regulated hematopoietic differentiation

被引：116

作者：

Yeh, Jing-Ruey J. ^{[1
,2
,3
]}

Munson, Kathleen M. ^{[1
,2
,3
]}

Elagib, Kamaleldin E. ^{[4
]}

Goldfarb, Adam N. ^{[4
]}

Sweetser, David A. ^{[2
,5
]}

Peterson, Randall T. ^{[1
,2
,3
]}

机构：

[1] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Dev Biol Lab, Charlestown, MA 02129 USA

[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

[3] MIT & Harvard, Broad Inst, Cambridge Ctr 7, Cambridge, MA 02142 USA

[4] Univ Virginia, Sch Med, Dept Pathol, Charlottesville, VA 22908 USA

[5] Massachusetts Gen Hosp, Div Pediat Hematol Oncol, Dept Pediat, Boston, MA 02114 USA

来源：

NATURE CHEMICAL BIOLOGY | 2009年 / 5卷 / 04期

关键词：

ACUTE MYELOID-LEUKEMIA; GLYCOGEN-SYNTHASE KINASE-3; PROSTAGLANDIN E-2; VALPROIC ACID; INTESTINAL POLYPOSIS; PROGENITOR CELLS; GENE DISRUPTION; KNOCKOUT MICE; BETA-CATENIN; COLON-CANCER;

D O I：

10.1038/nchembio.147

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

It has been proposed that inhibitors of an oncogene's effects on multipotent hematopoietic progenitor cell differentiation may change the properties of the leukemic stem cells and complement the clinical use of cytotoxic drugs. Using zebrafish, we developed a robust in vivo hematopoietic differentiation assay that reflects the activity of the oncogene AML1-ETO. Screening for modifiers of AML1-ETO-mediated hematopoietic dysregulation uncovered unexpected roles of COX-2- and beta-catenin-dependent pathways in AML1-ETO function. This approach may open doors for developing therapeutics targeting oncogene function within leukemic stem cells.

引用

页码：236 / 243

页数：8

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